Acute Stroke Management — Part 5: Subarachnoid Hemorrhage, TIA & Special Populations
SAH presentation, Hunt & Hess scale, WFNS grade, Fisher CT grading, aneurysm management, vasospasm prevention, DCI, TIA evaluation (ABCD2, dual antiplatelet), stroke mimics, posterior circulation, wake-up stroke, pregnancy, and pediatric stroke.
1. Subarachnoid Hemorrhage — Overview
Aneurysmal subarachnoid hemorrhage (aSAH) results from rupture of an intracranial saccular aneurysm, releasing blood into the subarachnoid space. It accounts for approximately 3-5% of all strokes but causes a disproportionate share of stroke-related morbidity and mortality, affecting a relatively younger population (mean age ~55 years). Approximately 10-15% of patients die before reaching the hospital, and overall case fatality is 25-50%. Among survivors, 30-50% experience significant long-term cognitive and functional disability.1 2
2. Clinical Presentation and Diagnosis
2.1 Classic Presentation
| Feature | Details |
|---|---|
| Headache | Sudden-onset, severe (“thunderclap”) headache, often described as “the worst headache of my life”; maximal intensity at onset; present in ~75-80% of cases |
| Loss of consciousness | Occurs in ~50% at onset; may be transient or prolonged |
| Nausea/vomiting | Common; related to acute ICP elevation |
| Meningismus | Neck stiffness, photophobia; develops over hours as blood irritates the meninges |
| Focal neurological deficits | Variable; cranial nerve palsies (especially CN III with posterior communicating artery aneurysm); hemiparesis if associated with intracerebral hematoma |
| Seizure | Occurs in ~10-25% at onset |
| Sentinel headache | ~20-50% of patients report a preceding severe headache days to weeks before rupture (“warning leak”) |
2.2 Diagnostic Workup
| Test | Timing/Role | Sensitivity |
|---|---|---|
| NCCT head | First-line; immediate | ~95-98% within 6 hours; ~93% at 12 hours; decreases to ~50% at 1 week |
| CT angiography (CTA) | If SAH confirmed or highly suspected; identifies aneurysm | ~95-98% for aneurysms ≥ 3 mm |
| Lumbar puncture | If CT is negative but clinical suspicion remains high | Gold standard for excluding SAH when CT is negative; look for xanthochromia (spectrophotometry preferred) and elevated RBC count that does not clear across tubes |
| Digital subtraction angiography (DSA) | Gold standard for aneurysm detection and treatment planning | ~99%; performed if CTA inconclusive or for treatment planning |
| MRI (FLAIR) | Alternative if LP not feasible; FLAIR sequence sensitive for subarachnoid blood | ~95% in acute phase |
2.3 LP Interpretation in Suspected SAH
| Finding | SAH | Traumatic Tap |
|---|---|---|
| RBC count across tubes | Does NOT significantly decrease (< 25% decrease) | Decreases sequentially (tube 1 > tube 4) |
| Xanthochromia | Present (yellow discoloration of CSF due to hemoglobin breakdown); requires ≥ 6-12 hours to develop | Absent |
| Opening pressure | Often elevated (> 20 cmH2O) | Usually normal |
| Spectrophotometry | Positive for bilirubin (most specific finding) | Negative |
Important: Xanthochromia takes approximately 6-12 hours to develop after SAH onset. If LP is performed very early (< 6 hours), xanthochromia may be absent even in true SAH. In this setting, an elevated RBC count that does not clear may be the only clue, and CTA should be performed regardless.
3. SAH Grading Scales
3.1 Hunt and Hess Scale
The Hunt and Hess scale is the most widely used clinical grading system for aSAH, based on clinical examination at presentation. It correlates with overall prognosis and guides management decisions.3
| Grade | Clinical Description | Approximate Mortality |
|---|---|---|
| I | Asymptomatic or mild headache, slight nuchal rigidity | ~1-5% |
| II | Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy | ~5-10% |
| III | Drowsiness, confusion, or mild focal neurological deficit | ~15-20% |
| IV | Stupor; moderate to severe hemiparesis; possibly early decerebrate posturing; vegetative disturbances | ~30-40% |
| V | Deep coma; decerebrate posturing; moribund appearance | ~50-70% |
3.2 World Federation of Neurosurgical Societies (WFNS) Grade
The WFNS scale provides a more objective grading based on the Glasgow Coma Scale (GCS) and the presence of motor deficits. It is the preferred scale in many neurosurgical centers and clinical trials.4
| WFNS Grade | GCS Score | Major Focal Deficit | Approximate Mortality |
|---|---|---|---|
| I | 15 | Absent | ~5% |
| II | 14-13 | Absent | ~9% |
| III | 14-13 | Present | ~20% |
| IV | 12-7 | Present or absent | ~33% |
| V | 6-3 | Present or absent | ~70% |
3.3 Fisher Scale and Modified Fisher Scale
The Fisher scale grades the amount and distribution of subarachnoid blood on the initial CT scan. It was originally developed to predict the risk of cerebral vasospasm. The modified Fisher scale provides improved prediction of delayed cerebral ischemia (DCI).5 6
Original Fisher Scale
| Grade | CT Findings | Risk of Vasospasm |
|---|---|---|
| 1 | No subarachnoid blood detected | Low (~20%) |
| 2 | Diffuse thin layer of subarachnoid blood (< 1 mm thickness) | Low-moderate (~25-30%) |
| 3 | Localized thick clot and/or vertical layer ≥ 1 mm | High (~65-70%) |
| 4 | Diffuse or no subarachnoid blood with intraventricular hemorrhage (IVH) or intracerebral hemorrhage (ICH) | Moderate (~35%) |
Modified Fisher Scale
| Grade | CT Findings | Risk of DCI |
|---|---|---|
| 0 | No SAH or IVH | Very low |
| 1 | Thin SAH, no IVH | Low (~15%) |
| 2 | Thin SAH with IVH | Moderate (~25%) |
| 3 | Thick SAH, no IVH | High (~30-35%) |
| 4 | Thick SAH with IVH | Very high (~40%) |
4. Acute SAH Management in the Emergency Department
4.1 Initial Stabilization
| Domain | Action |
|---|---|
| Airway | Intubate if GCS ≤ 8 or inability to protect airway; avoid hypoxia |
| Blood pressure | Target SBP < 160 mmHg (range 140-160 in most protocols) before aneurysm securing; nicardipine or labetalol infusion |
| Pain management | Aggressive analgesia — headache is severe; acetaminophen 1 g IV + opioid (morphine 2-4 mg IV or fentanyl 25-50 mcg IV); avoid NSAIDs (antiplatelet effect) |
| Seizure prophylaxis | Levetiracetam 1000-1500 mg IV load (preferred); or fosphenytoin 20 mg PE/kg; short-term use (≤ 72 hours) is reasonable; prolonged prophylaxis is NOT recommended1 |
| Anti-emetic | Ondansetron 4 mg IV; vomiting increases ICP |
| Avoid hyperthermia | Target normothermia; acetaminophen, cooling if needed |
| Avoid hyponatremia | Monitor sodium closely; SAH-associated hyponatremia (SIADH or cerebral salt wasting) is common and worsens edema |
| Venous thromboembolism prophylaxis | Intermittent pneumatic compression; pharmacologic prophylaxis after aneurysm secured |
| Stool softeners | Avoid straining (Valsalva maneuver increases ICP and rebleeding risk) |
4.2 Rebleeding Prevention
Rebleeding is the most dangerous early complication, occurring in approximately 4-6% of patients within the first 24 hours and carrying a mortality rate of 70-80%. The single most effective intervention to prevent rebleeding is early securing of the aneurysm.1 2
| Measure | Details |
|---|---|
| Early aneurysm treatment | Within 24 hours of presentation (ideally as soon as possible); endovascular coiling or surgical clipping |
| Blood pressure control | SBP < 160 mmHg before aneurysm securing |
| Antifibrinolytic therapy (short-term) | Tranexamic acid 1 g IV load then 1 g q8h or aminocaproic acid 4 g IV load then 1 g/h; use ONLY until aneurysm is secured (max 72 hours); reduces rebleeding risk but associated with increased DCI risk if used beyond 72 hours1 |
| Bed rest | Quiet, dark room; minimize stimulation; head of bed elevated 30° |
| Avoid anticoagulants/antiplatelets | Until aneurysm is secured |
4.3 Securing the Aneurysm — Coiling vs. Clipping
| Feature | Endovascular Coiling | Surgical Clipping |
|---|---|---|
| Mechanism | Platinum coils deployed into the aneurysm sac via microcatheter, promoting thrombosis | Metallic clip placed across the aneurysm neck via craniotomy, excluding it from circulation |
| ISAT trial evidence | Improved outcomes at 1 year (mRS 0-2: 76.3% coiling vs 63.3% clipping); lower mortality; less disability7 | Standard approach for over 50 years; definitive treatment |
| Preferred when | Posterior circulation aneurysms; elderly patients; poor-grade SAH (less invasive); favorable aneurysm morphology (small neck, accessible location) | Wide-neck aneurysms; MCA bifurcation aneurysms; aneurysms with incorporated branch vessels; associated large ICH requiring evacuation |
| Recurrence rate | Higher (~15-20% incomplete occlusion or recurrence) | Lower (~5-10% recurrence) |
| Complications | Intra-procedural rupture (2-5%); thromboembolic events (5-10%); coil migration | Retraction injury; vasospasm from surgical manipulation; higher rate of cognitive impairment |
| Long-term follow-up | Requires serial angiographic follow-up (MRA or DSA) | Less frequent follow-up needed |
Current practice: Endovascular coiling is the preferred treatment for most aneurysms, particularly posterior circulation aneurysms, based on the ISAT and subsequent BRAT trial data. Surgical clipping remains preferred for specific anatomical configurations and when associated ICH requires evacuation.
5. Vasospasm and Delayed Cerebral Ischemia (DCI)
5.1 Definitions
| Term | Definition |
|---|---|
| Angiographic vasospasm | Narrowing of cerebral arteries visible on angiography (DSA, CTA, or TCD); occurs in ~50-70% of SAH patients; peaks at days 5-14 |
| Clinical vasospasm | New focal neurological deficit or decreased level of consciousness attributable to vasospasm; occurs in ~20-30% of SAH patients |
| Delayed cerebral ischemia (DCI) | New focal neurological deficit and/or new cerebral infarction on CT/MRI attributable to vasospasm after other causes excluded; the clinically relevant endpoint; occurs in ~20-30% |
5.2 Nimodipine — The Only Proven Prophylactic Agent
Nimodipine, an L-type calcium channel blocker with preferential cerebrovascular effects, is the only pharmacologic agent proven to reduce DCI and improve outcomes after aSAH.8
| Parameter | Details |
|---|---|
| Dose | 60 mg PO/NG every 4 hours |
| Duration | 21 consecutive days (from SAH onset) |
| Evidence | British Aneurysm Nimodipine Trial: reduced poor outcomes from 33% to 20% (p < 0.05); reduced incidence of cerebral infarction |
| Mechanism | Reduces DCI — likely through neuroprotection and microvascular effects rather than large-vessel vasodilation |
| Hypotension | Most common side effect; if SBP drops < 100 mmHg, reduce dose to 30 mg q4h rather than discontinuing |
| Route | MUST be given enterally (PO or NG tube); IV nimodipine is not widely available in the US; do NOT administer oral solution intravenously (fatal hypotension) |
5.3 Detection of Vasospasm/DCI
| Method | Details | Threshold |
|---|---|---|
| Transcranial Doppler (TCD) | Non-invasive; daily monitoring starting day 3; measures mean flow velocity (MFV) in major intracranial arteries | MCA MFV > 120 cm/s = mild vasospasm; > 200 cm/s = severe; Lindegaard ratio (MCA MFV / extracranial ICA MFV) > 3 = vasospasm; > 6 = severe |
| Clinical examination | Serial neurological assessments at least every 1-2 hours during the high-risk period (days 3-14) | New focal deficit, declining consciousness, confusion — after excluding other causes (hydrocephalus, rebleeding, metabolic) |
| CTA | Assess for arterial narrowing | Sensitivity ~85% for moderate-severe vasospasm |
| CT perfusion | Assess for decreased perfusion in at-risk territories | CBF reduction, prolonged MTT/TTP in the setting of clinical deterioration |
| Digital subtraction angiography (DSA) | Gold standard; also allows endovascular treatment | Direct visualization of vasospasm; can proceed to intra-arterial treatment |
5.4 Treatment of Symptomatic Vasospasm/DCI
| Intervention | Details |
|---|---|
| Induced hypertension | First-line medical treatment; increase SBP by 20-30% above baseline (or target SBP 180-220 mmHg) using IV vasopressors (norepinephrine 0.05-0.3 mcg/kg/min or phenylephrine 0.5-5 mcg/kg/min); only after aneurysm is secured1 |
| Euvolemia maintenance | Maintain euvolemia with isotonic crystalloid (NS or LR); avoid hypervolemia (no longer recommended — HIMALAIA trial showed no benefit of prophylactic hypervolemia)9 |
| Intra-arterial vasodilators | Verapamil 5-20 mg, nicardipine 5-15 mg, or milrinone infused directly into the spastic artery via microcatheter during DSA |
| Balloon angioplasty | Mechanical dilation of spastic proximal large arteries (ICA, M1, A1, basilar) during DSA; provides sustained improvement; risk of vessel rupture (~1-2%) |
| Intrathecal vasodilators | Nicardipine pellets or intrathecal milrinone infusion; emerging therapies with limited high-quality evidence |
5.5 “Triple-H” Therapy — Historical Context
The traditional “triple-H” therapy (hypertension, hypervolemia, hemodilution) was the standard treatment for vasospasm for decades. Current evidence supports only the hypertension component. Prophylactic hypervolemia and hemodilution have NOT been shown to improve outcomes and may cause harm (pulmonary edema, dilutional anemia). Current recommendation: induced hypertension with maintenance of euvolemia.1 9
6. Other SAH Complications
| Complication | Timing | Management |
|---|---|---|
| Rebleeding | Highest risk first 24 hours | Early aneurysm treatment; BP control; short-term antifibrinolytics |
| Hydrocephalus (acute) | First 72 hours | EVD placement; ~20% of SAH patients require CSF diversion |
| Hydrocephalus (chronic) | Weeks to months | Ventriculoperitoneal (VP) shunt if persistent (~10-20% of SAH survivors) |
| Seizures | Acute or delayed | Acute: treat with benzodiazepines + antiepileptic loading; prophylaxis: levetiracetam × 72 hours; no long-term prophylaxis unless clinical seizures occur |
| Hyponatremia | Days 2-14 | Cerebral salt wasting (most common in SAH): volume replacement with normal saline + fludrocortisone 0.1-0.4 mg daily; SIADH: fluid restriction (but avoid hypovolemia which worsens vasospasm); differentiation is critical |
| Cardiac complications | Hours to days | Neurogenic stunned myocardium, Takotsubo cardiomyopathy, troponin elevation, arrhythmias; supportive care; usually reversible |
| Pulmonary edema | Days 1-7 | Neurogenic or cardiogenic; diuretics, positive pressure ventilation; avoid excessive fluid administration |
| DVT/PE | Days to weeks | SCDs immediately; LMWH prophylaxis after aneurysm secured (usually 24-48 hours post-treatment) |
7. Transient Ischemic Attack (TIA)
7.1 Definition
TIA is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The modern tissue-based definition emphasizes absence of infarction on diffusion-weighted MRI, rather than the older arbitrary time cutoff of 24 hours. Approximately 50% of episodes historically classified as TIA (symptoms < 24 hours) actually demonstrate DWI-positive infarction on MRI, and are reclassified as ischemic strokes under the current definition.10
7.2 ABCD2 Score
The ABCD2 score is a validated clinical prediction tool for stratifying the short-term risk of stroke following TIA. It is used to guide the urgency of diagnostic workup and the intensity of early secondary prevention.11
| Component | Criteria | Points |
|---|---|---|
| A — Age | ≥ 60 years | 1 |
| B — Blood pressure | SBP ≥ 140 and/or DBP ≥ 90 at initial evaluation | 1 |
| C — Clinical features | Unilateral weakness | 2 |
| Speech impairment without weakness | 1 | |
| Other | 0 | |
| D — Duration | ≥ 60 minutes | 2 |
| 10-59 minutes | 1 | |
| < 10 minutes | 0 | |
| D — Diabetes | Present | 1 |
Total score range: 0-7
| ABCD2 Score | 2-Day Stroke Risk | 7-Day Stroke Risk | 90-Day Stroke Risk | Risk Category |
|---|---|---|---|---|
| 0-3 | ~1% | ~1.2% | ~3.1% | Low |
| 4-5 | ~4.1% | ~5.9% | ~9.8% | Moderate |
| 6-7 | ~8.1% | ~11.7% | ~17.8% | High |
7.3 Limitations of the ABCD2 Score
- The ABCD2 score should NOT be used in isolation to determine disposition (admit vs. discharge); patients with low ABCD2 scores can still have high-risk etiologies (e.g., high-grade carotid stenosis, atrial fibrillation, intracranial stenosis)
- Any TIA patient with a known or suspected high-risk etiology should be hospitalized regardless of ABCD2 score
- Imaging findings (LVO, high-grade stenosis, DWI-positive lesion) take precedence over the ABCD2 score
7.4 Rapid TIA Workup
The 2019 guideline update recommends that TIA patients undergo rapid diagnostic evaluation, ideally within 24 hours:12
| Study | Urgency | Rationale |
|---|---|---|
| Brain MRI with DWI | Within 24 hours | Identifies acute infarction (reclassifies as stroke); determines tissue-based TIA vs. stroke |
| Neurovascular imaging (CTA or MRA) | Within 24 hours | Identifies LVO, carotid/intracranial stenosis, dissection |
| ECG | Immediate | Atrial fibrillation (present in ~5% at time of TIA) |
| Cardiac monitoring | ≥ 24 hours (inpatient) or outpatient Holter/event monitor × 30 days | Paroxysmal atrial fibrillation detected in ~5-15% with prolonged monitoring |
| Echocardiography | Within 48-72 hours | PFO, valvular disease, LV thrombus; TTE as initial screen; TEE if higher suspicion |
| Basic labs | Immediate | CBC, BMP, lipid panel, HbA1c, glucose, PT/INR |
7.5 Dual Antiplatelet Therapy for TIA/Minor Stroke
Two landmark trials established that short-term dual antiplatelet therapy (DAPT) reduces the risk of recurrent stroke after TIA or minor ischemic stroke:13 14
CHANCE Trial (Clopidogrel in High-Risk Patients with Acute Non-Disabling Cerebrovascular Events)
| Parameter | Details |
|---|---|
| Population | TIA (ABCD2 ≥ 4) or minor ischemic stroke (NIHSS ≤ 3) within 24 hours of onset |
| Region | China |
| Intervention | Clopidogrel 300 mg load then 75 mg/day + aspirin 75-300 mg load then 75 mg/day × 21 days, then clopidogrel monotherapy through day 90 vs. aspirin alone |
| Primary outcome | Recurrent stroke at 90 days: 8.2% (DAPT) vs 11.7% (aspirin); HR 0.68 (95% CI 0.57-0.81; p < 0.001) |
| Major hemorrhage | No significant difference (0.3% vs 0.3%) |
POINT Trial (Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke)
| Parameter | Details |
|---|---|
| Population | TIA (ABCD2 ≥ 4) or minor ischemic stroke (NIHSS ≤ 3) within 12 hours of onset |
| Region | International (mostly North America and Europe) |
| Intervention | Clopidogrel 600 mg load then 75 mg/day + aspirin 50-325 mg/day × 90 days vs. aspirin alone |
| Primary outcome | Major ischemic events at 90 days: 5.0% (DAPT) vs 6.5% (aspirin); HR 0.75 (95% CI 0.59-0.95; p = 0.02) |
| Major hemorrhage | Higher with DAPT: 0.9% vs 0.4% (HR 2.32; p = 0.02); excess risk appeared after day 21 |
Combined Evidence and Current Recommendation
| Recommendation | Details |
|---|---|
| Indication | TIA (ABCD2 ≥ 4) or minor ischemic stroke (NIHSS ≤ 3) presenting within 24 hours |
| Regimen | Aspirin 162-325 mg load + clopidogrel 300-600 mg load, then aspirin 81 mg + clopidogrel 75 mg daily |
| Duration | 21 days of DAPT (based on CHANCE; POINT data suggest benefit-risk optimal at 21 days) |
| After 21 days | Transition to single antiplatelet agent (aspirin or clopidogrel) |
| Alternative | Ticagrelor 180 mg load then 90 mg BID + aspirin × 30 days (THALES trial)15 |
8. Stroke Mimics
Approximately 25-30% of patients presenting with suspected acute stroke have an alternative (“mimic”) diagnosis. Rapid identification of stroke mimics is important to avoid unnecessary thrombolysis, though the risk of treating a mimic with alteplase is very low (sICH rate in mimics: ~0.5-1%).16
8.1 Common Stroke Mimics
| Mimic | Frequency Among Mimics | Key Distinguishing Features |
|---|---|---|
| Seizure / Todd paralysis | ~20% | Witnessed seizure activity; symptoms improve over hours; EEG may show epileptiform activity; focal deficit follows seizure and resolves |
| Migraine with aura | ~15% | History of migraine; “positive” symptoms (scintillating scotoma, paresthesias) that march/spread over minutes; headache follows; younger patients |
| Hypoglycemia | ~10% | Glucose < 50-60 mg/dL; symptoms resolve rapidly with glucose correction; check POC glucose immediately |
| Functional neurological disorder (conversion) | ~10% | Non-anatomical distribution; inconsistency on examination; positive neurological signs (Hoover sign, drift without pronation); normal imaging |
| Peripheral vertigo | ~5-10% | Benign paroxysmal positional vertigo or vestibular neuritis; HINTS exam (Head Impulse, Nystagmus, Test of Skew) negative for central cause |
| Brain tumor / mass lesion | ~5% | Subacute progression (days to weeks); headache with papilledema; identified on CT |
| Toxic / metabolic encephalopathy | ~5% | Diffuse rather than focal findings; history of medication changes, infections, organ failure |
| Syncope / presyncope | ~5% | Transient LOC with rapid recovery; no focal neurological deficit |
| Hypertensive encephalopathy / PRES | ~2% | Severely elevated BP; visual disturbance, seizures, headache; bilateral posterior white matter changes on MRI |
| Subdural hematoma | ~2% | History of trauma (may be minor/remote, especially in elderly or anticoagulated); crescent-shaped collection on CT |
| Demyelinating disease (MS flare) | ~1% | Younger patient; MRI with periventricular white matter lesions; CSF oligoclonal bands |
8.2 HINTS Examination for Central vs. Peripheral Vertigo
The HINTS exam is a bedside tool for differentiating central (stroke) from peripheral causes of acute vestibular syndrome (acute sustained vertigo with nystagmus). It has a sensitivity of ~97% and specificity of ~96% for central cause, outperforming early MRI in the first 24-48 hours.17
| Component | Peripheral (Benign) | Central (Dangerous — Think Stroke) |
|---|---|---|
| H — Head Impulse | Positive (corrective saccade present) | Negative (no corrective saccade — vestibular nucleus intact) |
| IN — Nystagmus | Unidirectional, horizontal; suppresses with fixation | Direction-changing or vertical or torsional; does NOT suppress with fixation |
| TS — Test of Skew | Negative (no vertical ocular misalignment) | Positive (vertical misalignment with alternate cover test) |
Interpretation: A negative head impulse test (normal VOR) + direction-changing nystagmus + positive test of skew = central pattern → high concern for posterior circulation stroke. Any single “central” finding warrants MRI and neurology consultation.
9. Special Populations
9.1 Posterior Circulation Stroke
Posterior circulation strokes (vertebrobasilar territory) account for approximately 20% of ischemic strokes and are among the most frequently missed diagnoses in the emergency department. The posterior circulation supplies the brainstem, cerebellum, thalamus, and occipital lobes.18
Key Clinical Features
| Feature | Details |
|---|---|
| Vertigo/dizziness | Most common presenting symptom; easily misdiagnosed as peripheral vertigo |
| Ataxia/gait instability | Cerebellar dysfunction; truncal ataxia (midline lesion) or limb ataxia (hemispheric lesion) |
| Diplopia | Cranial nerve III, IV, or VI palsy; or internuclear ophthalmoplegia |
| Dysarthria/dysphagia | Bulbar signs from medullary/pontine involvement |
| Visual field deficits | Homonymous hemianopia from occipital infarct |
| Crossed deficits | Ipsilateral cranial nerve + contralateral motor/sensory = classic brainstem localization |
| Decreased consciousness | Bilateral brainstem involvement; reticular activating system |
Diagnostic Challenges
| Issue | Details |
|---|---|
| Low NIHSS | The NIHSS poorly captures posterior circulation deficits; a patient with basilar artery occlusion and devastating quadriplegia may score very low on the NIHSS |
| CT sensitivity | NCCT has even lower sensitivity for posterior fossa ischemia (~7-16% in first 12 hours) due to bone artifact |
| MRI | DWI-MRI is the preferred imaging modality; sensitivity ~80-95% in the posterior fossa (lower than anterior due to artifacts) |
| CTA | Essential for identifying basilar artery or vertebral artery occlusion |
Management Principles
- Maintain a low threshold for CTA in any patient with acute vertigo, ataxia, or brainstem signs
- Use HINTS exam to differentiate central from peripheral vertigo
- NIHSS alone should NOT determine treatment eligibility for posterior circulation stroke
- IV thrombolysis criteria are the same as for anterior circulation
- EVT for basilar artery occlusion is supported by ATTENTION and BAOCHE trials (see Part 3)
9.2 Wake-Up Stroke and Unknown Onset
Approximately 15-25% of ischemic strokes are discovered upon awakening or have an unknown time of onset. Two imaging-based approaches allow treatment selection:19 20
| Approach | Selection Method | Treatment | Key Trial |
|---|---|---|---|
| DWI-FLAIR mismatch | DWI positive + FLAIR negative on MRI = likely onset < 4.5 hours | IV thrombolysis (alteplase 0.9 mg/kg) | WAKE-UP trial (mRS 0-1: 53% vs 42%; OR 1.61) |
| Perfusion mismatch | CTP or MRI-PWI demonstrating target mismatch (see DAWN/DEFUSE-3 criteria in Part 3) | EVT (if LVO present and mismatch criteria met) | DAWN (6-24h), DEFUSE-3 (6-16h) |
Current recommendation: All patients with wake-up stroke or unknown onset should undergo advanced imaging (MRI or CTP) to determine treatment eligibility. Time alone should not exclude patients from reperfusion therapy.
9.3 Stroke in Pregnancy and the Postpartum Period
Stroke in pregnancy is rare (approximately 12-34 per 100,000 pregnancies) but carries significant morbidity and mortality. Risk is highest during the third trimester and the postpartum period (first 6 weeks). Unique etiologies include eclampsia/preeclampsia, cerebral venous sinus thrombosis, postpartum angiopathy, and amniotic fluid embolism.21
| Consideration | Details |
|---|---|
| Imaging | NCCT is safe in pregnancy (low radiation dose to fetus with abdominal shielding); CTA is safe if indicated; MRI (without gadolinium) is preferred when feasible; gadolinium should be avoided unless absolutely necessary |
| IV thrombolysis | Alteplase does NOT cross the placenta in significant amounts; pregnancy is listed as a relative (NOT absolute) contraindication; in the setting of disabling stroke, the benefit-risk balance generally favors treatment after informed discussion12 |
| EVT | Radiation exposure during EVT can be minimized with abdominal shielding; risk-benefit analysis should consider maternal stroke severity |
| Eclampsia/PRES | IV magnesium sulfate is first-line for seizure prophylaxis; BP control with labetalol or nicardipine; delivery planning with obstetrics |
| Cerebral venous sinus thrombosis | Anticoagulation with LMWH or UFH is the standard treatment, even in the presence of hemorrhagic infarction; pregnancy/postpartum is the most common setting |
| Blood pressure targets | Severe hypertension (SBP ≥ 160 or DBP ≥ 110): treat urgently; labetalol (preferred), hydralazine, or nicardipine; avoid ACE inhibitors/ARBs (teratogenic) and nitroprusside (fetal cyanide toxicity) |
9.4 Pediatric Stroke
Pediatric stroke (neonatal through age 18) is uncommon (incidence ~1-13 per 100,000 children per year) but is among the top 10 causes of death in children. It frequently presents atypically and is often initially misdiagnosed.22
| Feature | Pediatric vs. Adult Stroke |
|---|---|
| Etiologies | Cardiac disease (congenital heart disease, including post-operative), sickle cell disease, moyamoya, arterial dissection (often post-traumatic), prothrombotic states, infections (varicella vasculopathy) |
| Presentation | Often atypical; may present with seizure (common in neonates), altered consciousness, behavioral change, or headache rather than classic focal deficits |
| Imaging | MRI with DWI is the preferred modality; CT may miss posterior fossa and small strokes |
| Treatment | No RCT evidence for IV thrombolysis in children; off-label use may be considered in selected cases per institutional protocol; EVT has been reported in case series for LVO; anticoagulation with UFH or LMWH for cardioembolic, dissection, or CVST etiologies |
| Sickle cell disease | Exchange transfusion to reduce HbS to < 30% is the primary treatment for acute stroke; chronic transfusion therapy reduces recurrence |
9.5 Cerebellar Stroke
Cerebellar stroke (ischemic or hemorrhagic) deserves special mention because of the risk of rapid deterioration due to posterior fossa swelling and brainstem compression.23
| Feature | Details |
|---|---|
| Presentation | Acute vertigo, nausea/vomiting, truncal ataxia (inability to sit or stand), headache, dysarthria; may be initially misdiagnosed as peripheral vertigo or gastroenteritis |
| Red flags | Inability to walk, severe headache, cranial nerve deficits, any brainstem signs |
| Imaging | NCCT may miss early cerebellar ischemia; MRI-DWI is preferred; CT is adequate for hemorrhage |
| Deterioration | Can be rapid and fatal; cerebellar edema → 4th ventricle compression → obstructive hydrocephalus → brainstem herniation |
| Surgical indications | Cerebellar hemorrhage > 3 cm or with brainstem compression/hydrocephalus → urgent posterior fossa decompression; cerebellar infarction with significant edema and hydrocephalus → suboccipital craniectomy and/or EVD |
| Thrombolysis/EVT | Standard criteria apply; posterior inferior cerebellar artery (PICA) and superior cerebellar artery (SCA) occlusions may be considered for EVT in selected cases |
10. Stroke Systems of Care
10.1 Stroke Center Certification Levels
| Level | Capabilities | Role |
|---|---|---|
| Acute Stroke Ready Hospital (ASRH) | NCCT; IV thrombolysis; telemedicine link to higher-level center; transfer protocols | Stabilize and treat with IV tPA; transfer for EVT if indicated |
| Primary Stroke Center (PSC) | NCCT, CTA; IV thrombolysis; stroke unit; neurology availability; quality improvement program | Definitive IV thrombolysis care; transfer for EVT if indicated; most common level |
| Thrombectomy-Capable Stroke Center (TSC) | All PSC capabilities + endovascular thrombectomy capability; neurointerventional availability | Can perform EVT; may transfer complex neurosurgical cases to CSC |
| Comprehensive Stroke Center (CSC) | All TSC capabilities + neurosurgery, neurointensive care, advanced imaging (CTP, MRI), 24/7 neurointerventional and neurosurgical availability | Highest level; manages the most complex cases including SAH, complex EVT, decompressive craniectomy |
10.2 Telestroke
Telestroke (telemedicine for stroke) extends stroke expertise to hospitals without on-site neurology, enabling remote NIHSS assessment, imaging review, and thrombolysis decision-making. Studies demonstrate that telestroke-guided IV thrombolysis produces outcomes comparable to on-site stroke team management and significantly increases thrombolysis rates at community hospitals.24
11. Early Secondary Prevention (All Ischemic Stroke/TIA)
| Intervention | Details |
|---|---|
| Antiplatelet therapy | Aspirin 160-325 mg within 24-48 hours of ischemic stroke onset (after excluding hemorrhage and if not on tPA); DAPT for TIA/minor stroke (see Section 7.5) |
| Statin therapy | High-intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) initiated during hospitalization; target LDL < 70 mg/dL (SPARCL trial evidence)25 |
| Anticoagulation (if atrial fibrillation) | DOAC (apixaban, rivaroxaban, edoxaban, or dabigatran) preferred over warfarin; timing of initiation: 4-14 days post-stroke depending on infarct size (1-3-6-12 day rule: TIA = day 1; small stroke = day 3; moderate = day 6; large = day 12-14)26 |
| Carotid revascularization | Symptomatic carotid stenosis ≥ 70%: carotid endarterectomy (CEA) or carotid artery stenting (CAS) within 2 weeks of TIA/minor stroke; stenosis 50-69%: CEA may benefit depending on patient factors27 |
| Blood pressure control | Target < 130/80 mmHg for long-term secondary prevention (after the acute phase); initiate or restart antihypertensives before discharge |
| Diabetes management | Screen for diabetes (HbA1c); optimize glycemic control |
| Lifestyle modification | Smoking cessation; exercise; Mediterranean diet; weight management; limit alcohol |
References
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